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[MiR-18a Can Regulate Chemotherapy Sensitivity of Leukemia Cell HL-60 to VP-16 and VCR by Targeting ATM].

作者信息

Xiao Yue, Hu Rong

机构信息

Department of Hematilogy, Yongchuan Hospital, Chongqing Medical University, Chongqing 420160, China.

Department of Pediatrics, Yongchuan Hospital, Chongqing Medical University, Chongqing 420160, China. E-mail:

出版信息

Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2015 Aug;23(4):999-1004. doi: 10.7534/j.issn.1009-2137.2015.04.017.

DOI:10.7534/j.issn.1009-2137.2015.04.017
PMID:26314433
Abstract

OBJECTIVE

To investigate the regulatory effects of miR-18a on chemotherapeutic sensitivity of leukemia cell HL-60 to VP-16 and VCR, and explore its molecular mechamism.

METHODS

The HL-60 PC DNA3.1-miR-18A cell line with stably overexpressing miR-18a was constructed and their sensitivity to VP-16 and VCR was detected. The luciferase reporter vector of ATM 3'UTR region was constructed and the targeting effect of miR-18a on ATM was identified. The expression level of ATM in HL-60 cells overexpressing miR-18a was detected by Western blot. The seusitivity of HL-60 cells with knockdown of ATM to VP-16 and VCR was detected by CCK-8 method. The ATM expression level in HL-60 cells with stably overexpression miR-18a after transfection of miR-18a inhibitor was detected by using Western blot and the sensitivity changes of these HL-60 cells to VP-16 and BCR were detected.

RESULTS

After overexpression of miR-18a, the viability of HL-60 cells treated with VP-16 and VCR of same concentration decreased; the detectiion of luciferase activity showed that the miR-18a could inhitit activity of luciferase reporter vector of ATM; the expression level of ATM in HL-60 cells was down-regulated after transfection with miR-18a; the cell viability decreased when HL-60 cells were treated with VP-16 and VCR after knockdown of ATM; the expression level of ATM was up-regulated and the cell viability decreased when HL-60 cells were treated with VP-16 and VCR after transfection with miR-18a inhibitor.

CONCLUSION

The miR-18a can regulated the sensitivity of leukemia HL-60 cells to VP-16 and VCR by targeting ATM.

摘要

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